<b>Results</b>: Three miRNAs (miR-137, miR-149-5p, and miR-561-5p) were identified to be associated with pulmonary metastasis in patients with HCC. miR-561-5p was most highly overexpressed in metastatic HCC tissues and high-metastatic-potential HCC cell lines.
Functionally, elevated TRIP13 facilitated cell proliferation, migration, invasion, and promoted cellular epithelial-mesenchymal transition (EMT) in vitro, while promote tumor growth and lung metastasis in vivo.
The results showed that both the mRNA and protein expression levels of MAT1 were elevated in osteosarcoma tissues with lung metastasis and metastatic lung tissues, particularly in the metastatic lung tissues, as compared to the osteosarcoma tissues without lung metastasis.
Chemotherapy-elicited EVs are enriched in annexin A6 (ANXA6), a Ca<sup>2+</sup>-dependent protein that promotes NF-κB-dependent endothelial cell activation, Ccl2 induction and Ly6C<sup>+</sup>CCR2<sup>+</sup> monocyte expansion in the pulmonary pre-metastatic niche to facilitate the establishment of lung metastasis.
Here, we have shown that aspirin dramatically reduced lung metastasis through inhibition of COX-1 while the cancer cells remained intravascular and that inhibition of platelet COX-1 alone was sufficient to impair metastasis.
Recent research published in the Journal of Pathology showed that genetic depletion of any of the NOX2 subunits Cyba, Cybb, Ncf1, Ncf2 and Ncf4 reduced the formation of lung metastases following intravenous injection of murine tumor cells.
Furthermore, the xenograft model indicated that miR-10b inhibited CRC cell growth and lung metastasis in vivo by targeting fibroblast growth factor 13 (FGF13).
Knockdown of miR-196a decreased transwell invasiveness, sphere formation, transendothelial invasion, and Slug, Twist, Oct4, and Sox2 expression, suppressed angiogenesis, and reduced sizes of xenotransplants and number of pulmonary metastasis.
In this study, we report on RUNX2/ p57 overexpression in 16 patients with primary non-small cell lung cancer and/or metastatic lung cancer associated with H3K27Ac at P1 gene promoter region.
The phosphorylation of sphingosine by sphingosine kinase enzymes SphK1 and SphK2 generates sphingosine-1-phosphate (S1P), which inhibits human chondrosarcoma cell migration, while SphK1 overexpression suppresses lung metastasis of chondrosarcoma.
In conclusion, GDF15 may promote osteosarcoma cell metastasis by regulating the TGF‑β signaling pathway, and serum GDF15 levels may be a potential prognostic and pulmonary metastasis‑predictive biomarker in osteosarcoma.